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British anti-Lewisite (BAL) (2,3-dimercaptopropanol; dimercaprol) is a metal chelator used clinically in conjunction with edetate calcium disodium (CaNa2EDTA) for lead encephalopathy and severe lead poisoning as well as other metals and metalloids.26,34 In severe lead poisoning, dimercaprol should precede the first dose of CaNa2EDTA by 4 hours to prevent redistribution of lead to the central nervous system (CNS).17,18 Dimercaprol has a narrow therapeutic index and is only administered intramuscularly (IM) because it is formulated in ­peanut oil. Oral succimer is used for patients with less severe lead toxicity. The roles for dimercaprol in arsenic and mercury poisoning have diminished since the development of succimer and the investigational chelator 2,3-dimercaptopropane sulfonate (DMPS). Dimercaprol remains indicated when the gastrointestinal tract is compromised.


Investigation into the use of sulfur donors as antidotes was precipitated by the World War II threat of chemical warfare with Lewisite (dichloro{2-chlorovinyl}arsine) and mustard gas (dichlorodiethyl sulfide {ClCH2CH2}2S).1,35,36 Both are vesicants that cause tissue damage when combined with protein sulfhydryl groups (Chap. 126).39 The investigations of Stocken and Thompson at Oxford led to the discovery of the dithiol 2,3-dimercaptopropanol (or BAL) that combines with Lewisite to form a stable 5-membered ring.44,47



Dimercaprol has a molecular weight of 124.2 Da and a specific gravity of 1.21.37 It is an oily liquid with only 6% weight/volume water solubility, 5% weight/volume peanut oil solubility, and a disagreeable odor. Aqueous solutions are easily oxidized and therefore unstable. Peanut oil stabilizes dimercaprol and benzyl benzoate (in the ratio of one part dimercaprol to 2 parts of benzyl benzoate), which renders the dimercaprol miscible in peanut oil.40

Mechanism of Action

The sulfhydryl groups of dimercaprol form chelates with certain metals, which are then excreted in the urine. Lead, arsenic, and inorganic mercury salts are the metals most amenable to chelation with dimercaprol.


The limited information available about the pharmacokinetics of dimercaprol was determined in the 1940s.1,28 Serum concentrations of dimercaprol peak about 30 minutes after IM administration, and distribution occurs ­rapidly.40,43 Within 2 hours after IM administration to rabbits, serum concentrations rapidly fall. Urinary excretion of dimercaprol metabolites, perhaps partially as glucuronic acid conjugates, accounted for nearly 45% of the dose within 6 hours and 81% of the dose within 24 hours.40,42 Very little is excreted unchanged in the urine.40 Dimercaprol is concentrated in the kidney, liver, and small intestine.38 Dimercaprol is also found in the feces, suggesting that an enterohepatic circulation exists. Hemodialysis is useful in removing the dimercaprol–metal chelate in ...

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